List of positional candidate genes after correcting for multiple testing and controlling the false discovery rate from genome wide association studies (GWAS) retrieved from the NHGRI-EBI Catalog of published genome-wide association studies (http://www.ebi.ac.uk/gwas/). The disease/trait examined in this study, as reported by the authors, was Response to TNF antagonist treatment. The EFO term response to TNF antagonist was annotated to this set after curation by NHGRI-EBI. Intergenic SNPS were mapped to both the upstream and downstream gene. P-value uploaded. This gene set was generated using gwas2gs v. 0.1.8 and the GWAS Catalog v. 1.0.1.
Authors:
C Liu, F Batliwalla, W Li, A Lee, R Roubenoff, E Beckman, H Khalili, A Damle, M Kern, R Furie, J Dupuis, RM Plenge, MJ Coenen, TW Behrens, JP Carulli, PK Gregersen
GWAS: rheumatoid arthritis, response to TNF antagonist
Description:
List of positional candidate genes after correcting for multiple testing and controlling the false discovery rate from genome wide association studies (GWAS) retrieved from the NHGRI-EBI Catalog of published genome-wide association studies (http://www.ebi.ac.uk/gwas/). The disease/trait examined in this study, as reported by the authors, was Response to TNF-alpha inhibitors in rheumatoid arthritis. The EFO term rheumatoid arthritis, response to TNF antagonist was annotated to this set after curation by NHGRI-EBI. Intergenic SNPS were mapped to both the upstream and downstream gene. P-value uploaded. This gene set was generated using gwas2gs v. 0.1.8 and the GWAS Catalog v. 1.0.1.
Authors:
SB Krintel, G Palermo, JS Johansen, S Germer, L Essioux, R Benayed, L Badi, M Ostergaard, ML Hetland
QTL associated with TNF-induced lethal shock susceptibility 2. This interval was obtained by using a fixed interval width of 25 Mbp around the peak marker (108575096)
Authors:
Staelens J, Wielockx B, Puimge L, Van Roy F, Gunet JL, Libert C
GWAS: rheumatoid arthritis, response to TNF antagonist
Description:
List of positional candidate genes after correcting for multiple testing and controlling the false discovery rate from genome wide association studies (GWAS) retrieved from the NHGRI-EBI Catalog of published genome-wide association studies (http://www.ebi.ac.uk/gwas/). The disease/trait examined in this study, as reported by the authors, was Response to anti-TNF therapy in rheumatoid arthritis. The EFO term rheumatoid arthritis, response to TNF antagonist was annotated to this set after curation by NHGRI-EBI. Intergenic SNPS were mapped to both the upstream and downstream gene. P-value uploaded. This gene set was generated using gwas2gs v. 0.1.8 and the GWAS Catalog v. 1.0.1.
Authors:
J Cui, EA Stahl, S Saevarsdottir, C Miceli, D Diogo, G Trynka, T Raj, MU Mirkov, H Canhao, K Ikari, C Terao, Y Okada, S Wedrén, J Askling, H Yamanaka, S Momohara, A Taniguchi, K Ohmura, F Matsuda, T Mimori, N Gupta, M Kuchroo, AW Morgan, JD Isaacs, AG Wilson, KL Hyrich, M Herenius, ME Doorenspleet, PP Tak, JB Crusius, IE van der Horst-Bruinsma, GJ Wolbink, PL van Riel, M van de Laar, HJ Guchelaar, NA Shadick, CF Allaart, TW Huizinga, RE Toes, RP Kimberly, SL Bridges, LA Criswell, LW Moreland, JE Fonseca, N de Vries, BE Stranger, PL De Jager, S Raychaudhuri, ME Weinblatt, PK Gregersen, X Mariette, A Barton, L Padyukov, MJ Coenen, EW Karlson, RM Plenge
GWAS: rheumatoid arthritis, response to TNF antagonist
Description:
List of positional candidate genes after correcting for multiple testing and controlling the false discovery rate from genome wide association studies (GWAS) retrieved from the NHGRI-EBI Catalog of published genome-wide association studies (http://www.ebi.ac.uk/gwas/). The disease/trait examined in this study, as reported by the authors, was Response to anti-TNF therapy in rheumatoid arthritis. The EFO term rheumatoid arthritis, response to TNF antagonist was annotated to this set after curation by NHGRI-EBI. Intergenic SNPS were mapped to both the upstream and downstream gene. P-value uploaded. This gene set was generated using gwas2gs v. 0.1.8 and the GWAS Catalog v. 1.0.1.
Authors:
K Honne, I Hallgrímsdóttir, C Wu, R Sebro, NP Jewell, T Sakurai, M Iwamoto, S Minota, D Jawaheer
QTL associated with TNF-induced lethal shock susceptibility 1. This interval was obtained by using a fixed interval width of 25 Mbp around the peak marker (110909916)
Authors:
Wielockx B, Staelens J, Puimge L, Vanlaere I, Van Roy M, van Lint P, Van Roy F, Libert C
QTL associated with TNF-induced lethal shock susceptibility 3. This interval was obtained by using a fixed interval width of 25 Mbp around the peak marker (84734943)
Authors:
Wielockx B, Staelens J, Puimge L, Vanlaere I, Van Roy M, van Lint P, Van Roy F, Libert C
List of positional candidate genes after correcting for multiple testing and controlling the false discovery rate from genome wide association studies (GWAS) retrieved from the NHGRI-EBI Catalog of published genome-wide association studies (http://www.ebi.ac.uk/gwas/). The disease/trait examined in this study, as reported by the authors, was Response to anti-TNF therapy in rheumatoid arthritis. The EFO term response to TNF antagonist was annotated to this set after curation by NHGRI-EBI. Intergenic SNPS were mapped to both the upstream and downstream gene. P-value uploaded. This gene set was generated using gwas2gs v. 0.1.8 and the GWAS Catalog v. 1.0.1.
Authors:
J Cui, EA Stahl, S Saevarsdottir, C Miceli, D Diogo, G Trynka, T Raj, MU Mirkov, H Canhao, K Ikari, C Terao, Y Okada, S Wedrén, J Askling, H Yamanaka, S Momohara, A Taniguchi, K Ohmura, F Matsuda, T Mimori, N Gupta, M Kuchroo, AW Morgan, JD Isaacs, AG Wilson, KL Hyrich, M Herenius, ME Doorenspleet, PP Tak, JB Crusius, IE van der Horst-Bruinsma, GJ Wolbink, PL van Riel, M van de Laar, HJ Guchelaar, NA Shadick, CF Allaart, TW Huizinga, RE Toes, RP Kimberly, SL Bridges, LA Criswell, LW Moreland, JE Fonseca, N de Vries, BE Stranger, PL De Jager, S Raychaudhuri, ME Weinblatt, PK Gregersen, X Mariette, A Barton, L Padyukov, MJ Coenen, EW Karlson, RM Plenge
List of positional candidate genes after correcting for multiple testing and controlling the false discovery rate from genome wide association studies (GWAS) retrieved from the NHGRI-EBI Catalog of published genome-wide association studies (http://www.ebi.ac.uk/gwas/). The disease/trait examined in this study, as reported by the authors, was Response to anti-TNF alpha therapy in inflammatory bowel disease. The EFO term response to TNF antagonist was annotated to this set after curation by NHGRI-EBI. Intergenic SNPS were mapped to both the upstream and downstream gene. P-value uploaded. This gene set was generated using gwas2gs v. 0.1.8 and the GWAS Catalog v. 1.0.1.
Authors:
MC Dubinsky, L Mei, M Friedman, T Dhere, T Haritunians, H Hakonarson, C Kim, J Glessner, SR Targan, DP McGovern, KD Taylor, JI Rotter
A signal transducing tumor necrosis factor receptor associated factor that is involved in TNF RECEPTOR feedback regulation. It is similar in structure and appears to work in conjunction with TNF RECEPTOR-ASSOCIATED FACTOR 2 to inhibit APOPTOSIS.
Generated by gene2mesh v. 1.1.1
A signal transducing tumor necrosis factor receptor associated factor that is involved in TNF RECEPTOR feedback regulation. It is similar in structure and appears to work in conjunction with TNF RECEPTOR-ASSOCIATED FACTOR 1 to inhibit APOPTOSIS.
Generated by gene2mesh v. 1.1.1
Tumor necrosis factor receptor family members that are widely expressed and play a role in regulation of peripheral immune responses and APOPTOSIS. The receptors are specific for TNF-RELATED APOPTOSIS-INDUCING LIGAND and signal via conserved death domains that associate with specific TNF RECEPTOR-ASSOCIATED FACTORS in the CYTOPLASM.
Generated by gene2mesh v. 1.1.1
A transmembrane-protein belonging to the TNF family of intercellular signaling proteins. It is a widely expressed ligand that activates APOPTOSIS by binding to TNF-RELATED APOPTOSIS-INDUCING LIGAND RECEPTORS. The membrane-bound form of the protein can be cleaved by specific CYSTEINE ENDOPEPTIDASES to form a soluble ligand form.
Generated by gene2mesh v. 1.1.1
Pathway Commons (PC) Geneset. This geneset contains genes that participate in the "HIV-1 Nef: Negative effector of Fas and TNF-alpha" pathway. This set was automatically constructed using the PC API.
The original source of this geneset is pid.
gene2pc v. 0.1.0
Last updated 2015.08.31
Pathway Commons (PC) Geneset. This geneset contains genes that participate in the "TNF receptor signaling pathway " pathway. This set was automatically constructed using the PC API.
The original source of this geneset is pid.
gene2pc v. 0.1.0
Last updated 2015.08.31
Kyoto Encyclopedia of Genes and Genomes (KEGG) Geneset. This geneset contains genes that participate in the "TNF signaling pathway" pathway. This set was automatically constructed using the KEGG API and enumerating all rat pathways.
gene2kegg v. 0.1.1
Last updated 2015.09.10
Kyoto Encyclopedia of Genes and Genomes (KEGG) Geneset. This geneset contains genes that participate in the "TNF signaling pathway" pathway. This set was automatically constructed using the KEGG API and enumerating all mouse pathways.
gene2kegg v. 0.1.1
Last updated 2015.09.10
Kyoto Encyclopedia of Genes and Genomes (KEGG) Geneset. This geneset contains genes that participate in the "TNF signaling pathway" pathway. This set was automatically constructed using the KEGG API and enumerating all human pathways.
gene2kegg v. 0.1.1
Last updated 2015.09.10
A 34 kDa signal transducing adaptor protein that associates with TUMOR NECROSIS FACTOR RECEPTOR TYPE 1. It facilitates the recruitment of signaling proteins such as TNF RECEPTOR-ASSOCIATED FACTOR 2 and FAS ASSOCIATED DEATH DOMAIN PROTEIN to the receptor complex.
Generated by gene2mesh v. 1.1.1
To further extend these studies to a large number of genes, mRNA profiles from IL-17A- and IL-17F-stimulated cells were studied using microarrays. The expression of several cell-specific markers was analyzed to characterize the population used in the experiment. Microarray-based comparison of IL-17A- and IL-17F-induced effects alone or in combination with TNF-. RA synoviocytes were stimulated with IL-17A or IL-17F (50 ng/ml) alone or in combination with TNF- (0.5 ng/ml) for 12 h. Gene products that showed a signal intensity of 30 or greater were considered as ex- pressed and genes with a 2-fold or greater change were considered as regulated.
Authors:
Zrioual S, Ecochard R, Tournadre A, Lenief V, Cazalis MA, Miossec P
Expression of IL-17 correlated best at day 14. Consistent with Fig. 4A, iNOS, part of the Tip-DC pathway, correlated best with long-term effects. Five genes appear among the top six in both analyses. They are highlighted in gray: IL-17, SERPINB3, S100A12 (Th17), iNOS (Tip-DC), IL-19 (other). Of the Th1 path- way, MX-1 is number 5 among the short-term effects and IL-8 is number 3 among the long-term effects.
Authors:
Haider AS, Lowes MA, Surez-Farias M, Zaba LC, Cardinale I, Khatcherian A, Novitskaya I, Wittkowski KM, Krueger JG
QTL associated with radiation pulmonary fibrosis 1. This interval was obtained by using a fixed interval width of 25 Mbp around the peak marker (35216590)
The production of 12 out of 27 measured factors was induced by CEsHUT including IL-1β, TNF and IL-1Ra. In contrast to sIL-1Ra production, that of IL-1β and TNF was inhibited by HDL, corroborating previous results. In addition, CEsHUT induced monocytes to produce factors involved in their localization, survival and differentiation such as CCL5 (RANTES), CCL2 (MCP-1), interferon-γ (IFNγ), granulocyte-macrophage colony-stimulating factor (GM-CSF), and macrophage-CSF (M-CSF). The production of the latter was moderate and it was not affected by HDL.
Authors:
Gruaz L, Delucinge-Vivier C, Descombes P, Dayer JM, Burger D
A widely expressed member of the TNF receptor-associated family that may play a role in neuronal development and EMBRYOGENESIS. Although TNF receptor-associated factor 4 does not strongly associate with TUMOR NECROSIS FACTOR RECEPTORS it may be a signaling partner with the GLUCOCORTICOID-INDUCED TNFR-RELATED PROTEIN that plays a role in the activation of JNK MITOGEN-ACTIVATED PROTEIN KINASES and NF-KAPPA B.
Generated by gene2mesh v. 1.1.1
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